Cardiogenic Shock Flashcards

1
Q

findings of PE that might indicate cardiogenic shock

A
  • history
  • crackles
  • S3
  • murmurs
  • dysrhythmia
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2
Q

what heart sound would you hear in someone in cardiogenic shock

A

s3; recall that this is due to rapid ventricular filling. might be heart if ventricle cannot expand or if preload is high.

Results from increased atrial pressure leading to increased flow rates, as seen in congestive heart failure, which is the most common cause of a S3. Associated dilated cardiomyopathy with dilated ventricles also contribute to the sound.

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3
Q

heart failure is failure of the circulatory system to either:

  1. provide adequate cardiac output

or

  1. to do so without operating at elevated filling pressures.

what “causes”/linked to congestive heart failure or cardiogenic shock?

A

1- cardiogenic shock

2- congestive heart failure

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4
Q

cardiogenic shock is due to low cardiac output. what symptoms are linked to this?

A

decreased LOC, cool extremities, low urine output, all linked to poor perfusion pressures and stuff.

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5
Q

six compoennts of proper oxygen deliver/perfusion system (PRRCAC)

A

! Preload ! Rate ! Rhythm ! Contractility ! Afterload ! Content

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6
Q

JVP estimates the pressure of the ___

A

right atrium

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7
Q
  • 48 year old male brought to ER acutely unwell
  • Had been at baseline until 3 weeks ago
  • Complained of exertional chest pain, accelerating
  • Thought it might be muscular so took last week off work and has been using daily ibuprofen
  • Found by wife this morning on living room floor ashen, clutching chest, gasping for air
  • Past medical history significant for diabetes, diet controlled

• Works in finance, heavy smoker

A

there is ST elevation in the II, III and AvF leads. BUT there is also st elevation in the V3-v6 leads. this indicates anterior MI STEMI

this might cause reduced cardiac output because of reduced function of the heart (reduced contractility) and thus he might have symptoms of cardiogenic shock

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8
Q
A
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9
Q

a person with actue MI has a primary heart problem of contractility. what is the compensatory repsonse?

A

rate, afterload compensation. thus tachychardia, cooling of extremities because of vaso contrcition causes increase in aftelroad as a response to poor cardiac output.

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10
Q

teatment of shock from actue mI

A

ABCs

  • standard therapy for acs; ASA, clopidogrel, anticoagulation.
  • prompt restoration of cornary blood flow via PCI
  • intotropic support( Inotropic agents are a group of medicines that affect the contraction of the heart muscle. Technically, inotropes can be divided into positive inotropes, which stimulate and increase the force of contraction of the heart muscle, and negative inotropes, which weaken the force of muscular contractions, decreasing how hard the heart has to work. However, clinically, if the word inotrope is used it typically refers to positive inotropes)– ex/ digoxin
  • mechanical support.
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11
Q

main causes of post MI shock

A
  • because of predominant LV failure (75&) or acute severe mitral regurgitation (8%)
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12
Q

predictors of mortality due to cardiogenic shock post MI

A

AGE is the biggest option.

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13
Q

how is shock related to early revascularization stratgeies?

A

the earlier the revascularization effort, the lower the mortality by shock.

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14
Q

inotropes increases ____. It is a standard of care in cardiogenic shock.

A

increaes contractility.

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15
Q

how does an intra-aortic balloon pump help with circulation

A
  • it gets inflated during diastole to facilitate coronary flow
  • it gets deflated during systole to reduce afterload on the left ventricle.
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16
Q

the impella is a ___ circulatory support effort that draws blood from the LV cavity and ejects under continuous flow into the aortic root in order to improve cardiac output

A

is a partial circulatory support.

17
Q

the tandem heart is a ___ circulatory support effort. what is it’s mechanism?

A

it’s a partial circulatory support effort.

Draws blood from the
left atrium through a catheter placed by trans-septal puncture
• Arterial cannula then placed percutaneously for outflow

18
Q
A
19
Q

ECMO complications

A
20
Q

note;

Additional contractility problems
• Fulminant myocarditis

• Tako tsubo - ‘stress cardiomyopathy’

  • Myocardial depression from sepsis (mixed shock state)
  • Peripartum cardiomyopathy
A
21
Q

• 82 yo M history of ‘remote heart attack’

• Has been having progressive fatigue and dyspnea on exertion over the past 6 months
• Symptoms have reached a point where he can no
longer walk even short distances and becomes lightheaded with effort
• Witnessed syncope today at the grocery store with minor head trauma, leading to 911 call
• Home medications - ASA, metoprolol

  • Alert, confused but obeys commands, small forehead laceration
  • HR ~ 20 bpm slightly irregular • BP ~ 70 mmHg • SpO2 98% on 2L of O2

• Extremities cool, minimal urine output when Foley placed

What’s going on with ECG?

A

this person is very bradycardic. the primary problem is the RATE.

  • compensatory repsonse will be to increase afterload or cool extremities.

bradycardia can be dangerous because the HR will limit cardiac output. (but tachycaria can be just as bad before it causes poor filling time thus reduced preload)

22
Q
A
23
Q

primary problem with ventricular tachycardia

A

rhythm/rate is too fast– reduces preload. thus there is a compensatory response (afterload- causing cool extremities)

24
Q

primary problem of fulminant myocarditis

A

contractility is affected. compensatory response is thus rate, incresaed afterload. Results in tachycardia and cool extremities.

25
Q

praimry problem of a conducting system disease

A
  • rate

compensation thus with afterload

26
Q

primary problem of heart block

A

rate– poor contraction because of reduced signal propagation

  • elevated afterload is a compnesatory repsonse resulting in cool extremities
27
Q

2 types of shock that causes a hgih JVP

A

cardiogenic

obstructive